Nutrients (protein, carbohydrates and fats) have traditionally been thought of as fuels simply providing the energy for cellular metabolic activity. According to the classic view, if nutrients are available, then anabolic pathways are activated, and if nutrients are not available, catabolic pathways are activated. However, it is becoming increasingly clear that nutrient effects on bone cells (stem cells, osteoblasts and osteoclasts) are complex, some nutrients promote bone formation, whereas others interfere with bone formation or actually promote bone break down. At an organ level, nutrient intake can suppress bone breakdown and modulate the activity of the calcium/vitamin D/parathyroid hormone axis. At a cellular level, nutrient intake can impact cellular energetics either through a direct mechanism (binding or uptake of the nutrient into the cell) or indirect (by elevating nutrient-related hormones such as insulin, insulin-like growth factor 1 or incretin hormones). It is also becoming clear that within a nutrient class (for example, protein), individual components (that is, amino acids) can have markedly different effects on cell function and impact bone formation. The focus of this review will be on one nutrient class in particular, dietary protein. As the prevalence of inadequate dietary protein intake increases with age, these findings may have translational implications as to the optimal dietary protein content in the setting of age-associated bone loss.